Here using a middle cerebral rodent infarct model the following conclusions can be drawn:
1. Melatonin protects injured but recoverable stunned brain cells. (Antioxidant effect)
2. Exercise increases connectivity of neurons that survive. (BDNF effect)
3. Both together protect via Melatonin inhibiting Reactive oxygen species directly, inhibiting inflammasome indirectly; and, Exercise increasing BDNF directly and thereby increasing nerve connectivity via dendrites, synaptic message amplification, cellular energy metabolism, hippocampal neurogenesis allowing reintegration of the command and control of these cells for future recovery and conscious use.
The brain of the brain is the hippocampus. It learns, predicts and motivates the rest of the brain.
Adult neurogenesis is what makes BDNF the memory chemical.
Adult neurogenesis is what makes BDNF the positive mood chemical.
BDNF promotes distal command and control systems primarily as a hormone effect with neuron connections as target organ.
BDNF promotes cellular energy efficiency as a paracrine effect with energy sensing and promotion as targets.
Pivotal role of melatonin plus exercise as a neuroregenerator following focal cerebral ischemic injury
- Sookyoung Park1,2,
- Seunghoon Lee2,3 and
- Yonggeun Hong2,3,4
+ Author Affiliations
Among the numerous studies related to therapeutic mechanism following stroke, neurogenesis plays a critical role. Therefore, we hypothesized that combination therapy with melatonin and exercise might exert on the neurogenesis after focal cerebral ischemia. Sprague-Dawley rats were randomly divided into control (Con) and middle cerebral artery occlusion (MCAo) groups treated vehicle (Veh), melatonin (MT), exercise (EX), and melatonin with treadmill exercise (MT+Ex). MCAo-induced neurological deficits were improved by melatonin with and without exercise. Furthermore, we confirmed the expression of NeuN and Doublecortin were significantly reduced in MCAo+Veh, while melatonin with without exercise attenuated these alterations. The expression of BDNF, in particular mature-BDNF was increased, but not pro-BDNF after MCAo. These changes were reduced at chronic phase of MCAo. GFAP expression was increased in lesion area of MCAo+Veh, then melatonin with and without exercise decreased these changes. By histological examination, MCAo-induced infarction volumes were reduced by melatonin with and without exercise. We found that neurite length from perikaryon was markedly diminished than control rat. However, melatonin plus exercise promotes neurite outgrowth from penumbra to infarct core lesion. Thus, these results demonstrate that melatonin plus exercise could contribute to neuroregeneration and support the potential use for stroke. Funding: 2014R1A1A3051724, 2013 Post-Doctoral Research Program of Inje University, 2012R1A1A2005089, 2013R1A2A2A01067169, KGM4611512
